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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The C2H2 zinc-finger protein SYD-9 is a putative posttranscriptional regulator for synaptic transmission
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The C2H2 zinc-finger protein SYD-9 is a putative posttranscriptional regulator for synaptic transmission

机译：C2H2锌指蛋白SYD-9是一种可能的转录后转录调节子，用于突触传递

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摘要

Communication between neurons is largely achieved through chemical synapses, where neurotransmitters are released from synaptic vesicles at presynaptic terminals to activate postsynaptic cells. Exo- and endocytosis are coordinated to replenish the synaptic vesicle pool for sustained neuronal activity. We identified syd-9 (syd, synapse defective), a gene that encodes multiple C2H2 zinc-finger domain-containing proteins specifically required for synaptic function in Caenorhabditis elegans. syd-9 loss-of-function mutants exhibit locomotory defects, a diffuse distribution of synaptic proteins, and decreased synaptic transmission with unaffected neurodevelopment. syd-9 mutants share phenotypic and ultrastructural characteristics with mutants that lack synaptic proteins that are required for endocytosis. syd-9 mutants also display genetic interactions with these endocytotic mutants, suggesting that SYD-9 regulates endocytosis. SYD-9 proteins are enriched in the nuclei of both neuron and muscle cells, but their neuronal expression plays a major role in locomotion. SYD-9 isoforms display a speckle-like expression pattern that is typical of RNA-binding proteins that regulate premRNA splicing. Furthermore, syd-9 functions in parallel with unc-75 (unc, uncoordinated), the C. elegans homologue of the CELF/BrunoL family protein that regulates mRNA alternative splicing and processing, and is also required specifically for synaptic transmission. We propose that neuronal SYD-9 proteins are previously uncharacterized and specific post-transcriptional regulators of synaptic vesicle endocytosis.
机译：神经元之间的交流主要是通过化学突触实现的，其中神经递质从突触前末端的突触小泡释放，以激活突触后细胞。胞外和内吞作用被协调以补充突触囊泡池以维持持续的神经元活性。我们鉴定了syd-9（syd，突触缺陷），该基因编码秀丽隐杆线虫突触功能特别需要的多个包含C2H2锌指结构域的蛋白质。 syd-9功能丧失的突变体表现出机能缺陷，突触蛋白的分散分布以及突触传递减少，而神经发育未受影响。 syd-9突变体与缺乏内吞所需突触蛋白的突变体具有表型和超微结构特征。 syd-9突变体还显示出与这些胞吞突变体的遗传相互作用，表明SYD-9调节胞吞作用。 SYD-9蛋白富含神经元和肌肉细胞的核，但它们的神经元表达在运动中起主要作用。 SYD-9同工型显示斑点样表达模式，这是调节premRNA剪接的RNA结合蛋白的典型特征。此外，syd-9与unc-75（unc，uncoordinated）（CELF / BrunoL家族蛋白的秀丽隐杆线虫同源物）并行运行，调节cDNA的剪接和加工，并且突触传递也特别需要。我们提出，神经元SYD-9蛋白是先前未表征的和突触小泡内吞作用的特定转录后调节剂。

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